Far Lateral Lumbar Disc Herniations

CHAPTER PREVIEW

CHAPTER SYNOPSIS:

Far lateral disc herniations (FLDHs) of the lumbar spine represent a relatively rare condition in which the site of neural element compression is located lateral to the neuroforamen. In contrast with posterolateral herniations that typically involve the traversing nerve root, extraforaminal herniations characteristically affect the exiting root, resulting in signs and symptoms consistent with a monoradiculopathy. As with all types of lumbar disc herniations, the majority of these lesions may be adequately treated with conservative measures such as activity modifications, physical therapy, medications, or spinal injections; however, selected patients who do not respond successfully to nonoperative therapies may be expected to respond favorably to surgical decompression, either through an open approach or using a minimally invasive technique.

KEY POINTS:

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FLDHs are uncommon, comprising between 3% and 12% of all disc bulges occurring in the lumbar spine.
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Extraforaminal herniations are most frequently observed at the L4-L5 and L5-S1 levels.
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Although the specific constellation of signs and symptoms is dependent on the nerve root that is being compressed, patients with FLDHs may often present with more severe radicular complaints and neurologic findings with less axial low back pain compared with those with paracentral disc herniations.
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Establishing the definitive diagnosis of an extraforaminal disc herniation requires advanced cross-sectional imaging modalities such as computed tomography (CT) or magnetic resonance imaging (MRI), which remains the study of choice for visualizing these lesions.
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Virtually all FLDHs initially may be treated without surgery, especially because they are unlikely to cause any significant compression of the spinal cord, conus medullaris, or cauda equina given their location outside of the spinal canal.
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Surgery may be indicated for those who have not responded positively to a suitable regimen of conservative therapies; the ideal candidate for decompression is a patient who has unilateral leg symptoms with or without axial back pain, a positive tension sign, and evidence of a concordant lesion at the appropriate level on CT or MRI studies.
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The presence of a far lateral disc lesion with foraminal or intracanalicular components (i.e., a double herniation) may be associated with persistent radicular symptoms and poor clinical outcomes after operative intervention through a lateral intermuscular approach.

SURGICAL PEARLS:

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A lateral intermuscular (i.e., Wiltse) approach may be preferable for extraforaminal herniations because this exposure allows for decompression of the nerve root with minimal disruption of the facet joint and other stabilizing structures of the spine.
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For far lateral herniations that extend into the foramen or spinal canal, a partial or complete facetectomy may be required to gain access to any intraforaminal or intracanalicular disc fragments.
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As with any spinal operation, it is absolutely critical that the correct level be identified and confirmed with appropriate imaging studies.
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In general, the nerve root is mobilized superiorly to gain access to the extraforaminal disc herniation.
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Because the intertransverse window is more limited at L5-S1, a portion of the sacrum may need to be removed to adequately visualize the L5 nerve root and the adjacent extraforaminal disc herniation.

SURGICAL PITFALLS:

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Performing a discectomy in conjunction with a facetectomy for extraforaminal herniations may increase the risk for postoperative instability; therefore, in these cases, a concomitant arthrodesis may be indicated to reduce the incidence of progressive iatrogenic instability, especially in individuals with preexisting spondylolisthesis or scoliotic deformities.
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When positioning the patient for surgery, make sure that the abdomen is free of any pressure to decrease venous bleeding.
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With a Wiltse approach, the plane between the multifidus and longissimus muscles should be carefully developed to minimize the disruption of the surrounding soft tissues and vasculature.
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Elevation of the intertransverse membrane is initiated where it inserts into the cephalad transverse process and is continued in an inferomedial direction; because the location of the nerve root may be altered by the disc bulge, this membrane must be meticulously dissected free of the underlying psoas muscle to avoid injuring the neural elements.
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During the decompression, care should be taken to avoid excessive manipulation of the nerve root or dorsal root ganglion, which may otherwise result in postoperative neuropathic pain.

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Lumbar nerve root compression represents a significant cause of back and/or leg pain in the general population. While compression of the neural elements may occur as a result of a number of pathologic changes such as a hypertrophied facet joint or vertebral osteophyte, the most common cause of lumbar radiculopathy remains disc herniations. A herniated nucleus pulposus (HNP) may be classified according to its anatomic location with respect to the foramen, that is, intracanalicular, foraminal, or extraforaminal. The relevant structures which form the borders of the foramen are the vertebral body and intervertebral disc anteromedially, the facet joint posterolaterally, and the pedicles of the cephalad and caudad vertebrae superiorly and inferiorly, respectively.

Extraforaminal, also referred to as “far lateral” disc herniations (FLDHs), are known to be relatively rare, with reported prevalence rates ranging from 3% to 12% of all lumbar HNPs. However, it is possible that the prevalence of FLDH in the lumbar spine may be underestimated in the literature because of the poor sensitivity and specificity of older imaging modalities such as myelography.

FLDH may be purely extraforaminal in nature or may occur in conjunction with other pathology within the foramen or spinal canal. Although conflicting reports have been published in the literature regarding the most common levels involved, the largest series reported that this disorder was most often observed at L4-L5 and L5-S1, followed by L3-L4, and only infrequently at L2-L3. The incidence of FLDH increases again in the proximal lumbar spine, a finding that has been attributed to smaller interpedicular distance of these segments. Consequently, herniation of nucleus pulposus material may be more likely to occur at these levels because a greater percentage of the disc space is lateral to the foramina. This condition also tends to be more prevalent in older individuals, with a peak incidence in the sixth decade of life.

In 1974, Abdullah et al. first described the existence of FLDH in the lumbar spine. Since that time, the clinical features of this diagnosis have been well characterized and are generally consistent with a monoradiculopathy involving the exiting nerve root; in contrast, disc herniations located within the spinal canal will typically affect the traversing nerve root. For instance, a far lateral lesion at L4-L5 will contact the L4 root once it has already exited the foramen, whereas a posterolateral herniation at this level will characteristically impinge on the L5 root as it travels distally as part of the cauda equina. A unique situation arises at L5-S1, where the exiting L5 nerve root may actually be compressed between the FLDH and the sacral ala.

Several studies have reported that patients with FLDH may often present with more severe radicular complaints and neurologic deficits with little or no axial low back pain compared with those with paracentral lesions. Postacchini and Montanaro suggest that these differences in symptomatology may be accounted for by the fact that, although FLDHs may apply pressure to the nerve root, they do not contact the posterior longitudinal ligament or the anterior surface of the thecal sac as other types of herniations do. More recently, the dorsal root ganglia have been implicated as a potential source of neuropathic pain in individuals with FLDH; in addition to directly compressing this structure, these lesions may also trigger an inflammatory response resulting in further dysfunction of the nerve root. In one series of patients with either posterolateral, intraforaminal, or extraforaminal lumbar HNP, Ohmori et al. observed significantly greater pain scores and lower walking capacity in those with FLDH. Furthermore, the authors were able to establish a direct correlation between the degree of dorsal root ganglion compression and the severity of radicular pain in the patients with FLDH.

As with paracentral herniations, the constellation of symptoms resulting from FLDH is dependent on the specific nerve root that is involved. HNP affecting the L1-4 roots may cause pain or numbness originating in the hip and radiating to the thigh or knee, loss of proximal muscle strength, as well as a positive femoral nerve stretch test. The clinical presentation of patients with more caudal extraforaminal herniations (e.g., at the L5-S1 level) would be expected to be more consistent with “classic” sciatica and may include pain or numbness traveling distally down the entire lower extremity, weakness of the extensor hallucis longus or tibialis anterior muscles, and a positive straight leg raising test. However, a great deal of variability exists in the published rates of positive tension signs associated with FLDH, ranging from 35% to 78%.

Although certain subtle differences may exist between the history and physical examination findings of an extraforaminal herniation and those of HNP based elsewhere in the spinal canal, these lesions may not be readily differentiated from each other using clinical criteria alone. Any individual with persistent signs and symptoms consistent with a FLDH should be evaluated with a diagnostic study that provides cross-sectional anatomic data of the lumbar spine such as computed tomography (CT) or magnetic resonance imaging (MRI). MRI is currently the advanced imaging modality of choice for identifying FLDHs, which are best visualized on parasagittal reconstructions ( Fig. 15–1 ). In particular, myelography is no longer considered to be a reliable method for identifying extraforaminal herniations because the sensitivity of this technique is limited by the flow of the contrast material; these lesions may easily escape detection if the radiopaque dye fails to extravasate through the neuroforamina and visualize the far lateral space.

INDICATIONS AND CONTRAINDICATIONS

As with all types of lumbar HNP, most patients with extraforaminal disc herniations may initially be managed conservatively with any number of nonsurgical modalities such as activity modification, physical therapy, anti-inflammatory drugs, oral steroids, or spinal injections. Given their anatomic location outside of the spinal canal, FLDH is unlikely to bring about any significant compression of the spinal cord, conus medullaris, or cauda equina, which would warrant more emergent operative decompression. The reported success rates of nonoperative therapies for FLDH vary between 10% and 70%, although many of these studies are relatively small and are retrospective in nature. However, data have been reported that support the use of injections consisting of local anesthetic and steroids as an adjunctive therapy for alleviating the radicular pain related to symptomatic extraforaminal herniations. Weiner and Fraser followed a series of individuals who underwent transforaminal selective nerve root injections for FLDHs. In this investigation, 27 of 30 of these subjects were found to have immediate relief, which was largely maintained over time, whereas only 3 patients ultimately required surgery.

Operative intervention may be reasonable option to consider for cases of extraforaminal herniations that prove to be refractory to at least a 6- to 8-week regimen of conservative measures. The ideal candidate for a decompressive procedure is an individual who exhibits a predominance of unilateral leg pain with or without associated axial back pain, a positive tension sign on physical examination, and evidence of a concordant lesion at the appropriate level on confirmatory CT or MRI studies.

Multiple surgical techniques have been described for the treatment of FLDH, all of which may be classified into three discrete categories: (1) completion of a hemilaminectomy with partial or complete facetectomy through a midline skin incision; (2) development of the intertransverse interval in conjunction with a lateral intermuscular (i.e., Wiltse) approach; and (3) a combination of these strategies for lumbar HNP with both intracanalicular and extraforaminal components. For isolated FLDH, it may be preferable to utilize the intertransverse plane because this exposure allows for the removal of pathologic disc material with minimal disruption of the posterior osteoligamentous structures, which are critical for the maintenance of spinal stability. In cases where fragments of the FLDH are known to extend into the foramen or spinal canal, a portion of the lateral facet joint may need to be excised to gain full access to the disc herniation. Nevertheless, facetectomy must be performed judiciously, particularly in individuals who are at increased risk for development of progressive iatrogenic instability, such as those with obvious motion on preoperative dynamic lateral radiographs, incompetence of the facet joints, or deformities in either the sagittal or coronal planes. For instance, symptomatic FLDH at the level of an isthmic or degenerative spondylolisthesis may require excision of the entire inferior articular facet to ensure that the nerve root is sufficiently mobile; in this situation, a concomitant arthrodesis may be indicated to prevent further progression of the slip. Patients with scoliosis may already have preexisting foraminal stenosis secondary to abnormal rotation of the spinal column; therefore, a FLDH present at the apex of a curve may require a more extensive decompression that would also justify the addition of an instrumented fusion in an attempt to minimize the incidence of postoperative instability.

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